[Prognosis in pediatric traumatic brain injury. A dynamic cohort study]. / Pronóstico del traumatismo craneoencefálico pediátrico. Estudio de una cohorte dinámica.

BACKGROUND: traumatic brain injury is a main cause of hospital admission and death in children. Our objective was to identify prognostic factors of pediatric traumatic brain injury. METHODS: this was a dynamic cohort study of traumatic brain injury with 6 months follow-up. The exposition was: mild or moderate/severe traumatic brain injury, searching for prognosis (morbidity-mortality and decreased Glasgow scale). Relative risk and logistic regression was estimated for prognostic factors. RESULTS: we evaluated 440 patients with mild traumatic brain injury and 98 with moderate/severe traumatic brain injury. Morbidity for mild traumatic brain injury was 1 %; for moderate/severe traumatic brain injury, 5 %. There were no deaths. Prognostic factors for moderate/severe traumatic brain injury were associated injuries (RR = 133), fractures (RR = 60), street accidents (RR = 17), night time accidents (RR = 2.3) and weekend accidents (RR = 2). Decreased Glasgow scale was found in 9 %, having as prognostic factors: visible injuries (RR = 3), grown-up supervision (RR = 2.5) and time of progress (RR = 1.6). CONCLUSIONS: there should be a prognosis established based on kinetic energy of the injury and not only with Glasgow Scale.

Introducción: en los niños con traumatismo, las lesiones craneoencefálicas son las principales causas de hospitalización y muerte. El objetivo de esta investigación fue identificar los factores pronóstico del traumatismo craneoencefálico en los niños. Métodos: cohorte dinámica con seis meses de seguimiento. El trauma craneoencefálico se estratificó como leve o moderado-severo, se identificó morbilidad y se realizó evaluación con la escala de coma de Glasgow. Se estimó riesgo relativo (RR) y regresión logística para factores pronóstico. Resultados: se identificaron 440 pacientes con trauma craneoencefálico leve y 98 con moderado-severo; se observó morbilidad en 1 y 5 %, respectivamente. No hubo defunciones. Los factores pronóstico para el trauma moderado-severo fueron los siguientes: lesiones relacionadas (RR = 133), fracturas (RR = 60), accidentes en la calle (RR = 17), horario nocturno (RR = 2.3) y fin de semana (RR = 2). Se presentó deterioro en la puntuación de Glasgow en 9 %, con los siguientes factores pronóstico: lesiones visibles (RR = 3), supervisión por adulto (RR = 2.5) y tiempo de evolución (RR = 1.6). Conclusiones: en los niños con trauma craneoencefálico debe establecerse el pronóstico según la energía cinética de la lesión y con la escala Glasgow.

Protective in vivo effect of curcumin on copper genotoxicity evaluated by comet and micronucleus assays.

Curcumin is a phytochemical with antiinflammatory, antioxidant and anticarcinogenic activities. Apparently, curcumin is not genotoxic in vivo, but in vitro copper and curcumin interactions induce genetic damage. The aim of this study was to test if in vivo copper excess induces DNA damage measured by comet and micronucleus assays in the presence of curcumin. We tested 0.2% curcumin in Balb-C mice at normal (13 ppm) and high (65, 130 and 390 ppm) copper ion concentrations. The comet and micronucleus assays were performed 48 hr after chemical application. Comet tail length in animals treated with 0.2% curcumin was not significantly different from the control. Animals exposed to copper cations (up to 390 ppm) exhibited higher oxidative DNA damage. Curcumin reduced the DNA damage induced by 390 ppm copper. We observed statistically significant increase in damage in individuals exposed to 390 ppm copper versus the control or curcumin groups, which was lowered by the presence of curcumin. Qualitative data on comets evidenced that cells from individuals exposed to 390 ppm copper had longer tails (categories 3 and 4) than in 390 ppm copper + curcumin. A statistically significant increase in frequency of micronucleated erythrocytes (MNE/10000TE) was observed only in 390 ppm copper versus the control and curcumin alone. Also cytotoxicity measured as the frequency of polychromatic erythrocytes (PE/1000TE) was attributable to 390 ppm copper. The lowest cytotoxic effect observed was attributed to curcumin. In vivo exposure to 0.2% curcumin for 48 hr did not cause genomic damage, while 390 ppm copper was genotoxic, but DNA damage induced by 390 ppm copper was diminished by curcumin. Curcumin seems to exert a genoprotective effect against DNA damage induced by high concentrations of copper cations. The comet and micronucleus assays prove to be suitable tools to detect DNA damage by copper in the presence of curcumin.